The antitumor mechanism of PD-1/PD-L1 inhibitors (e.g., pembrolizumab, camrelizumab, atelizumab) involves disrupting immune evasion strategies employed by cancer cells, thereby reactivating T-cell-mediated tumor destruction.[66] PD-1 is a checkpoint receptor on activated T-cells that suppresses their activity when engaged. This evidence concerns the gene CD274 and neoplasm.